Deprenyl (Selegiline) is a monoamine oxidase B inhibitor used to treat Parkinson’s Disease by inhibiting the metabolism of the neurotransmitter dopamine. Deprenyl produces a neuroprotective effect in vitro by increasing the expression of the anti-apoptotic gene bcl2 in cultured mammalian neurons. Deprenyl also increases the lifespan of rats by an unknown mechanism. Here we characterize deprenyl-induced developmental delay in C. elegans, a novel effect of this compound, and begin to deduce its mechanism of action. The nematode BCL2 ortholog (CED-9) regulates developmental rates of C. elegans, and our lab identified CED-9 as a potential candidate for the deprenyl-induced developmental delay that we observed. Populations of wild type (N2) and ced-9 gain of function (gf) C. elegans were synchronized to the same age and exposed to either vehicle (water) or 1.0 mM deprenyl. Developmental rates and lifespan of the organisms in each condition were scored. The deprenyl and ced-9(gf) combination have a synergistic effect on developmental delay with no apparent change in average lifespan, suggesting that deprenyl treatment either further increases CED-9 activity in the ced-9(gf) mutant or works independently of CED-9 activity to delay C. elegans development.

Deprenyl induces synergistic developmental delay in C. elegans ced-9(gf) mutants

ACS Spring Meeting 2021

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